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首页> 外文期刊>Journal of Molecular Biology >Preferential binding sites for interferon regulatory factors 3 and 7 involved in interferon-A gene transcription.
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Preferential binding sites for interferon regulatory factors 3 and 7 involved in interferon-A gene transcription.

机译：干扰素A基因转录中涉及的干扰素调节因子3和7的优先结合位点。

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摘要

Transcription of the murine interferon-A4 (IFN-A4) gene is mediated by a virus responsive element (VRE-A4) located in the promoter proximal [-120 to -43] region. VRE-A4 contains four DNA modules (A to D) which cooperate for maximal IFN-A4 activation following virus infection. The differential expression between the highly expressed IFN-A4 and the weakly inducible IFN-A11 gene promoters is essentially due to point mutations within the C and D modules of the virus-responsive element VRE-A11. We now demonstrate that in murine L929 and human 293 cells, transcription factors IRF-3 and IRF-7, which are potent activators of virus-induced type I IFN transcription, differentially affect IFN-A4 and IFN-A11 promoter activities. Using electrophoretic mobility shift assays and DNase I footprinting data, our studies demonstrate that the AB modules correspond to a preferential site for IRF-7, whereas the C module is preferentially recognized by IRF-3. Furthermore, transfection of reporter constructs driven by four copies of different GAAANN hexameric motifs found within VRE-A4 indicates that the NN residues of these hexameric sequences define the preferential binding sites for IRF-3 or IRF-7. Together, these experiments clarify the molecular basis for differential expression of IFN-A genes following virus infection by delineating the sequence requirements for IRF association with the virus responsive elements of the IFN-A genes.
机译：鼠干扰素-A4（IFN-A4）基因的转录是由位于启动子近端[-120至-43]区的病毒反应元件（VRE-A4）介导的。 VRE-A4包含四个DNA模块（A到D），它们在病毒感染后协同最大程度地激活IFN-A4。高度表达的IFN-A4和弱诱导型IFN-A11基因启动子之间的差异表达主要是由于病毒反应元件VRE-A11的C和D模块内的点突变。现在，我们证明在鼠L929和人293细胞中，转录因子IRF-3和IRF-7是病毒诱导的I型IFN转录的有效激活剂，它们差异地影响IFN-A4和IFN-A11启动子的活性。使用电泳迁移率变动分析和DNase I足迹数据，我们的研究表明AB模块对应于IRF-7的优先位点，而C模块则被IRF-3优先识别。此外，由在VRE-A4中发现的四个不同GAAANN六聚体基序的四个拷贝驱动的报告基因构建体的转染表明，这些六聚体序列的NN残基定义了IRF-3或IRF-7的优先结合位点。总之，这些实验通过描绘IRF与IFN-A基因的病毒反应元件相关的序列要求，阐明了病毒感染后IFN-A基因差异表达的分子基础。

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